The factors and mechanisms that regulate osteoclast-induced inflammatory bone loss are complex. The authors of this Review provide an overview of osteoclast regulation in the context of inflammatory bone loss and rheumatoid arthritis and provide insights into potential treatment strategies.

Childhood-onset SLE is characterized by high disease activity, severe organ damage and substantial treatment challenges. The authors of this Review provide an update on the advances in the understanding of the pathogenesis of childhood-onset SLE in the past decade, emphasizing the need for more research to improve outcomes.

Circulating cell-free DNA (cfDNA) and cfDNA fragmentation signatures are emerging as promising non-invasive biomarkers for various indications, most notably cancer. New analysis of cfDNA fragmentation in autoimmunity highlights potential links to cancer, as well as the promise of these tools for improved understanding and clinical care of autoimmune disease.

The results of the phase II DAHLIAS trial support the development of the neonatal Fc receptor blocker nipocalimab for the treatment of Sjögren disease.

Findings reveal that inhibiting cytosolic phospholipase A₂ in chondrocytes could be a potential therapeutic target for degenerative joint diseases.

A new population-based study suggests that sodium–glucose cotransporter-2 (SGLT2) inhibitors — originally developed for glycaemic control — reduce the risk of autoimmune rheumatic diseases.

In a phase III placebo-controlled trial, the addition of telitacicept to standard therapy led to increased clinical response rates for people with systemic lupus erythematosus.

Biallelic loss-of-function mutations in PLD4, as identified in five patients with SLE, lead to Toll-like receptor-driven hyperactivation of type I interferon, immune cell expansion and autoimmunity.

Progress has been astonishing, but the need for personalized care can only be addressed through a universal focus on diversity and equity in rheumatology research.